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Atropine esterase

There were also some observational foreruimers. In 1932, Snyder (3) described a heritable disability of some people to taste phenylthiocarbamide. In 1943, Savin and Glick (4) noticed a genetic lack of atropine esterase in some rabbits these animals died while eating belladoima leaves, whereas most rabbits were not affected. These cases were perceived as isolated observations they preceded the definition of pharmacogenetics but they helped later investigators to establish pharmacogenetics as a science. [Pg.4]

A large number of new tropanyl esters and other related compounds have been prepared, with the purpose of contributing further structure-pharmacological activity relationships. Inter alia, para-substituted tropanyl benzoates (for studies of the substrate specificity of atropine esterase), benzazocines (narcotic antagonists) from 6-hydroxytropinone, 5-aryl-furan-2-carboxylic esters of pseudotropine (local anaesthetics), 2,4,5-trimethylpyrrole-3-carboxylic acid... [Pg.50]

Y. Kitamura, H. Miura and M. Sugii, Alkaloid composition and atropine esterase activity in callus and differentiated tissue of Duboisia myoporoides R.Br., Chem. Pharm. Bull., 33 (1985) 5445-5448. [Pg.271]

Hydrolysis of succinylcholine in human plasma is genetically controlled patients deficient in plasma esterases remain paralysed for several hours after a moderate dose of succinylcholine, whereas normal patients recover within a few minutes (see p. 614). Procaine is hydrolysed rapidly in human plasma but slowty in other species. Rabbit plasma, but not that of dog or man, rapidly de-esterifies the anticoagulant ethyl bis (4-hydroxycoumarinyl) acetate. Rabbit plasma has a very active atropine esterase which is not found in human plasma this activity is under strict genetic control. [Pg.580]

The answer is local anesthetic properties it can block the initiation or conduction of a nerve impulse. It is biotransformed by plasma esterases to inactive products. In addition, cocaine blocks the reuptake of norepinephrine. This action produces CNS stimulant effects including euphoria, excitement, and restlessness Peripherally, cocaine produces sympathomimetic effects including tachycardia and vasoconstriction. Death from acute overdose can be from respiratory depression or cardiac failure Cocaine is an ester of benzoic acid and is closely related to the structure of atropine. [Pg.159]

Eserine blocks acetylcholine esterase. This alkaloid may be used to decrease possible negative side effects connected to the use of other drugs, for example that of atropine. [Pg.185]

Since the therapy with esterase inhibitors is not without risk a poisoning with atropine or other parasympatholytic drugs is treated only symptomatically. [Pg.296]

Standard therapy of OP poisoning consists of the administration of a combination of atropine, oxime, and diazepam with other supportive measures when necessary. However, the possibility of addition of purified enzymes such as AChE, ChE, CarbE, and A-esterases to this therapeutic scheme has been considered and preliminary experiments in animals have shown much better protective effect after addition of exogenous enzymes. In this respect, protective effects of AChE, ChE, and CarbE are based on formation of covalent conjugates or phosphory-lated enzymes in the stoichiometric ratio 1 1. Capacity for binding of these enzymes is limited by the number of active sites on the enzyme to which OP molecules can be bound. This means that more enzymes have to be administered in order to achieve better detoxification of OPs which may not always be possible due to adverse effects. This can also be infiuenced by differences in the extent of spontaneous reactivation of these enzymes inhibited by OP. [Pg.803]

The failure to find C02 In the expired air of the mice Indicates that the tropic acid moiety in the atropine molecule Is not metabollzed ln accord with the finding that labeled tropic acid Itself was excreted without loss In the urine. The finding of atropine but no tropic acid In the urine of the mice Indicates that hydrolysis of the ester did not occur rapidly. The latter finding was somewhat unexpected because an esterase capable of hydrolysing atropine is present In the livers of many vertebrate species, although It or a similar enzyme appears In the sera of only a few species (93-95). This enzyme Is also able to hydrolyze L hyoscyamine, troplnyl benzoate, and caramlphen (95). [Pg.151]

Main et al. (M5) found high concentrations of a butyrylcholine esterase, of relative molecular mass 83,000 daltons, in pooled rabbit serum. This was unexpected, since rabbit serum is classed with those mammalian sera that have low cholinesterase activities (A25, E2). Substrate specificity confirmed that the enzyme was a butyrylcholine esterase. Moreover, the active site concentration of the enzyme was five times that found for pooled horse serum, which is a rich source of the enzyme. The known fact that some rabbits can metabolize atropine, whereas others are unable to do so, can be explained by the presence or absence of serum atropinase, which is a genetic trait. Perhaps the subunit-sized butyrylcholine esterase is characteristic of some rabbits, but absent in others This seems probable according to Ellis (E9) and Koelle... [Pg.48]

In F. hepatica and schistosomes, the nicotinic agonist carbachol is a more potent agonist of muscle relaxation/inhibition than is ACh (perhaps because of its insensitivity to esterase). Muscarine is ineffective. Application of the muscarinic antagonist atropine stimulates increased muscle tone, contraction and/or motility and reverses the paralysis induced by carbachol and ACh (9-11, 13, 32). The stimulatory effect of atropine and the ability of eserine (a cholinesterase inhibitor) to relax muscle have fed several investigators to suggest that a tonic release of transmitter from cholinergic cells may be... [Pg.261]

Savin, P. B. and Glick, D. (1943) Hydrolysis of atropine by esterase present in rabbit serum. Proc. Natl. Acad. Sci. USA 29, 55. [Pg.12]

The best animal model for studying the effects of exposure to organophosphates is the chicken.29,30 Extensive studies have been performed to elucidate the mechanism of action that causes OPIDN and to screen new organophosphate insecticides for this effect.29,30 The exact mechanism of action is still unknown, but much evidence suggests that the inhibition of neurotoxic esterase in nerve tissue is involved.31 Administration of oximes and atropine has no effect on the production of this neurotoxicity.32... [Pg.232]

Hydrolysis is accomplished by esterases found in plasma or liver microsomes, e.g. carboxylesterase, arylesterase and acetylesterase, cholinesterase. Hasma esterases have been detected which will hydrolyse procaine [88—90], succinyl-choline [89], tromexan (rabbit) [91], atropine (rabbit) [92], cocaine (rabbit) [93], which are not necessarily identical with similar enzymes in liver [94]. Deamidation, e.g. of procaine amide is much slower than de-esterification [95-98]. [Pg.32]


See other pages where Atropine esterase is mentioned: [Pg.71]    [Pg.61]    [Pg.319]    [Pg.71]    [Pg.61]    [Pg.319]    [Pg.404]    [Pg.107]    [Pg.262]    [Pg.35]    [Pg.359]    [Pg.41]    [Pg.414]    [Pg.397]    [Pg.128]    [Pg.404]    [Pg.423]    [Pg.957]    [Pg.986]    [Pg.32]    [Pg.666]    [Pg.1316]    [Pg.140]    [Pg.146]    [Pg.205]    [Pg.335]    [Pg.336]    [Pg.659]    [Pg.240]    [Pg.633]    [Pg.662]    [Pg.156]    [Pg.166]    [Pg.490]    [Pg.69]    [Pg.143]    [Pg.478]   
See also in sourсe #XX -- [ Pg.580 , Pg.619 ]




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